Bone Function And Repair Flashcards
What are the functions of bone?
Mechanical=protect tissue + organs, provide framework for body shape, form basis of levers involved in movement
Synthetic=heamopoiesis (hold and protect red bone marrow)
Metabolic=mineral storage, fat storage (yellow marrow), acid-base Homeostasis (absorb/release alkaline salts)
What is endochondral ossification?
Formation of long bones from a cartilage template. So tinted lengthening is by ossification at Epiphyseal plates (appositional growth at edges)
What is inter-membranous ossification?
The formation of bone from cluster of MSC in the centre of bone-trabecular bone
(Interstitial growth in middle of bone)
Also contributes to thickening of the bone at periosteal edges in appositional growth
How do long bones develop?
They require a cartilage template in order to develop by endochondral ossification
(Continued lengthening by ossification at epiphyseal plates)
How do flat bones develop?
Skull, scapula, rib, mandible etc
Develop directly from Mesenchymal tissue, by intra-membranous ossification.
(Formation of bone from clusters of MSC in centre of bone)
How does intramembranous ossification work? Using parietal bone as example.
Mineral deposits within the many trabecular radiate outward from a central point, this is the early primary ossification centre.
What happens to a bony spicule once its first formed by ossification?
Once bony spicule has formed, then osteoblasts, osteocytes and osteoclasts remodelling it in the same way regardless if which method of ossification was used initially
Where does intramembranous ossification take place?
Within the condensations of Mesenchymal tissue and not by replacing pre-existing hyaline cartilage templates.
What is appositional growth?
Growth from the edges of bone, pushes cartilage at edge up and away.
What is inter membranous growth?
Growth directly from Mesenchymal cells, from the middle of the bone outwards.
What are the stages of intramembranous ossification?
1) Mesenchymal stem cells (MSC) form a tight cluster
2) The MSC’s transform into osteoprogenitor cells and then transform into osteoblasts
3) Osteoblats lay down an osteoid (ECM containing type 1 collagen)
4) The osteoid mineralises to form rudimentary bone tissue spicules
5) The spicules join to form trabeculae, which merge to woven bone
6) Trabeculae replaced by the lamella of mature compact bone
What does the HAversian canal in mature bone contain? Where is it located?
Blood vessels, lymph vessel and neurones
Located in the osteon of the cell
What’s the difference in arrangement between immature and mature bone?
Immature has osteocytes in random arrangents
Mature has osteocytes ranged in lamellae of osteons
Resorption canals in mature bone run parrelel to the osteon’s long axes
What is cancellous bone?
Forms a network of fine bony columns/ plates to combine strength with lightness. The spaces are filled with bone marrow.
What is compact bone?
Forms the external surfaces of bones and comprises 80% of skeletalm ass
What is the difference between the structure of compact and cancellous bone?
Compact-has Haversian (verticals) canals and Volkmann’s (horizontal) canals which carry blood vessels, lymph vessels and nerves. Has circular Osteons with interstitial lamella (circular layers)
Cancellous-concentric rings of osteocytes, collagen fibres laid in lines following gravity. No canals, this provides more room for bone marrow. The canals aren’t needed as the bone cels are surrounded by marrow/fat so receive their nutrients etc this way.
What features allow bone to resist fractures?
They have great tensile and compressive strength, also a degree of flexibility.
The main force lines are through the cortical bone, down the length as the body weight goes this way.
What feature gives the bones the strength/compressibility/flexibility to resist fracture?
The lamella (layers) are though to be able to slip relative to each other to resist fracture. Only excessive load or an unusual direction causes fracture.
How is bone thickened and remodelled?
Osteons remodel themselves to thicken bone, they mainly rethicken along the force lines as this is where additional strength is needed.
Why does exercise effect bone strength?
As it constantly changes the force lines, the bone is constantly remodelled to add strength along more and more places, it increases the Osteon activity.
Inactivity increases bone resorption (1/3 lost when immobile). This is because the force lines don’t change so no new bone I layer down
What factors in the bone itself effect bone stability?
Activity of osteocytes (Osteoid recycling)-can act as osteoblasts and lay down scavenged Osteoid into lamella. Or act as osteoclasts and degrade bone a little.
Activity of Osteoblasts (bone deposition)-stimulated by calcitonin, GH, oestrogen,testosterone, thyroid hormones and Vitamin A.
Activity of Osteoclasts (bone resorption)- Increased by PTH (releases Ca+ into blood), Calcitonin blocks PTH at its receptor.
How does nutrition effect bone stability?
Vitamin D3 (absorbed from gut or synth by skin)-produces calcitrol for Ca2 absorption.
Vitamin C- synthesis of collagen
Vitamin K and B12- synthesis of bone proteins
Give an brief overview of fracture repair steps.
1) Heamatoma formed + granulation arises
2) Procallus of granulation tissue replaced by fibrocartilaginous callus in which bony trabeculae develop
3) Endochondrial and intramembranous ossification giver is ti bony callous of cancellous bone
4) Cencellous bone replaced by cortical bone nail remodelling complete
Describe step one of fracture repair (heamatoma formation).
Blood vessels in bone + periosteum break. A mass of clotted blood form. Bone cells at fracture edge die. Swelling and inflammation occurs (as granulocytes enter site). Phagocytose cells and osteoclasts remove dead and damaged bone tissue. Macrophages will eventually remove blood clot.
Describe step 2 of fracture repair. (Fibrocartilaginous callus formation)
New blood vessel infiltrate the fracture heamatoma. A new procallus of granulation tissue develops. Fibroblasts produce collagen fibres to span the break. Others differentiate into chondroblasts that make sleeve of hyaline cartilage.
AT same time, osteoblasts invade fracture site and begin reconstruction of trabecular bone. (They come from nearby periosteum and endosteum.
Describe step 3 of fracture repair (bony callous formation).
Within a week new bone trabeculea appear in the fibrocartilaginous callus. The trabeculae develop as the former fibrocartilaginous callus is converted to a hard callous of cancellous bone.
Epichondrial ossification replaces all cartilage with cancellous bone. Intramembranous ossification produces new cancellous bone in any gaps.
This continues about 2 months until very firm union formed across fracture
Describe stage 4 of fracture repair (bone remodelling).
Cancellous bone beings to be remodelled into compact bone, especially n the prior cortical region.
The material building from the outside of bone and inwards toward medullary cavity is removed by osteoclasts.
Final shape of remodelled area is same as original bone as it responds to same mechanical stressors.
What 2 stages happens in the bone remodelling stage to create new osteons
1) osteoclasts make a wide tunnel in the bone (cutting cone)
2) Ostoeblasts make a smaller tunnel or cortical bone (closing cone)
Forms new osteons (circular layers)
What is Oteogenesis Imperfecta?
A mutation in COL1A gene
Incorrect production of collagen 1 fibres (they have no alpha helix so the protein bends)
This causes weak bones and increased fracture risk
Short height and stature and blue sclera
Mainly effects neonates and children (usually as they don’t live to adulthood)
What is rickets?
Mainly effects children Vitamin D deficiency Poor calcium mobilisation Ineffective mineralisation Weakened bone development Soft bones Short height and structure Painful to walk Characteristic bowed legs (too soft 4 weight bearing)
What is Osteomalacia?
Adults “rickets”
VItamin D deficiency - lower mineralisation + increase Osteoid
Increased calcium resorption
Caused by:
Kidney disease (NO VIT D activates)
No sunlight (no VIT D synth)
Surgery on stomach/intestine (no VIT D absorbed)
Drugs (phenytoin prevents VIT D absorption)
What are the 2 types of PRIMARY Osteoporosis?
Type 1- occurs in post menopause women, due to increased osteoblasts number, loss of oestrogen.
Type 2- occurs in older people (both genders), due to loss of osteoblasts function (senile osteoporosis), loss of both oestrogen and androgens.
What is SECONDARY Osteoporosis?
Due to:
Drug therapy (corticosteroids)
Processes effecting bone remodelling (malnutrition, prolonged immobilisation or weightlessness)
Metabolic bone disease (hyperparathyridism (tumour), metastatic cancers)
What is Osteoporosis?
When aging result in incomplete filling of osteoclast resorption bays (leaving dips and holes in bone)
Ie loss of bone tissue in veritable bodies
What are some modifiable risk factors for Osteoporosis?
Calcium intake-if insufficient more likely to suffer (700mg/day for post menopause)
Exercise-immobilisation leadsto accelerated bone loss. Activity needed to maintain bone mass. Astronauts often get Osteoporosis.
Cigarette smoking in women is correlated with incidence of osteoporosis.
What is Achondroplasia?>
Inherited mutation in FGF3 receptor gene
FGF promotes college formation from cartilage ( endochondral ossification affected, intramembranous ossification unaffected)
Short stature but normal head and torso as long bones cannot lengthen properly
